AIM: Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) has a wide range of biological functions, including anti-inflammation. In this study, we investigated the inhibitory effects of PPAR-gamma on transforming growth factor beta1 (TGF-beta1)-induced interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) expression in renal tubular epithelial cells (HK-2). METHODS: HK-2 cells were pretreated with 15d-PGJ2 or troglitazone (TGL) and then treated with TGF-beta1. Expression of MCP-1 and IL-8 was measured using real-time PCR and ELISA. RESULTS: Treatment with 5 ng/mL TGF-beta1 for 24 h increased both MCP-1 and IL-8 mRNA and protein levels in HK-2 cells. Both 15d-PGJ2 at 2.5 and 5 micromol/L and TGL at 2.5 micromol/L exhibited inhibitory effects on TGF-beta1-induced MCP-1 expression. Additionally, 15d-PGJ2 at 2.5 and 5 micromol/L and TGL at 2.5 micromol/L inhibited TGF-beta1-induced expression of IL-8. CONCLUSION: PPAR-gamma agonists (15d-PGJ2 and TGL) could inhibit the TGF-beta1-induced expression of chemokines in HK-2 cells. Our results suggest that PPAR-gamma agonists have the potential to be used as a treatment regimen to reduce inflammation in renal tubulointerstitial disease.
AIM: Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) has a wide range of biological functions, including anti-inflammation. In this study, we investigated the inhibitory effects of PPAR-gamma on transforming growth factor beta1 (TGF-beta1)-induced interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) expression in renal tubular epithelial cells (HK-2). METHODS: HK-2 cells were pretreated with 15d-PGJ2 or troglitazone (TGL) and then treated with TGF-beta1. Expression of MCP-1 and IL-8 was measured using real-time PCR and ELISA. RESULTS: Treatment with 5 ng/mL TGF-beta1 for 24 h increased both MCP-1 and IL-8 mRNA and protein levels in HK-2 cells. Both 15d-PGJ2 at 2.5 and 5 micromol/L and TGL at 2.5 micromol/L exhibited inhibitory effects on TGF-beta1-induced MCP-1 expression. Additionally, 15d-PGJ2 at 2.5 and 5 micromol/L and TGL at 2.5 micromol/L inhibited TGF-beta1-induced expression of IL-8. CONCLUSION:PPAR-gamma agonists (15d-PGJ2 and TGL) could inhibit the TGF-beta1-induced expression of chemokines in HK-2 cells. Our results suggest that PPAR-gamma agonists have the potential to be used as a treatment regimen to reduce inflammation in renal tubulointerstitial disease.
Authors: Lu Yang; Yan Wang; Aobulikasimu Nuerbiye; Ping Cheng; Jin-Hui Wang; Rena Kasimu; Hong Li Journal: Int J Mol Sci Date: 2018-05-29 Impact factor: 5.923